Hemodynamics of Increased Intra-abdominal Pressure

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Abstract
The hemodynamic interaction of acute hypovolemia and halothane anesthesia in dogs with increased intra-abdominal pressure caused by i.p. instillation of N2, N2O and CO2 was studied. During normovolemia and just basal pentobarbital anesthesia, the response to increase of intra-abdominal pressure to 40 torr consisted of a 35% decrease in cardiac output, which was equal to the decrease in magnitude of inferior vena caval blood flow. During basal pentobarbital anesthesia the addition of halothane anesthesia (1 MAC [minimum anesthetic concentration]) in combination with hypovolemia (15% blood volume loss) depressed the pre-inflation cardiac output more than addition of halothane anesthesia alone or induction of hypovolemia alone. During each of these conditions, superimposition of increased intraabdominal pressure to 40 torr caused a further 26-43% decrease in cardiac output compared with the pre-inflation value. The greatest cardiovascular depression occurred when the animals were both hypovolemic and anesthetized with halothane. There was no difference in the responses to increased intra-abdominal pressure with the differeent inflating gases at any time. In the presence of halothane anesthesia or hypovolemia, induction of pneumoperitoneum may cause severe cardiovascular depression.

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